Neuroprotective effect of osmotin against ethanol-induced apoptotic neurodegeneration in the developing rat brain

Naseer, Muhammad Imran; Ullah, Ikram; Narasimhan, Meena L.; Lee, H Y; Bressan, Ray A.; Yoon, Gwang Ho; Yun, Dae‐Jin; Kim, M O

doi:10.1038/cddis.2014.53

Cited by 56 publications

(43 citation statements)

References 55 publications

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“…Early indications suggest that in embryonic neurons, NF‐κB translocation stimulated by tumour NF alpha promotes neuron survival, possibly by inducing the expression of anti‐apoptotic proteins such as Bcl‐2 and Bcl‐x . The important contribution of Bcl‐2 to apoptotic processes in hippocampal neurons is now especially well documented . Moreover, several studies have linked the reduction of Bcl‐2 expression to the neuronal damage in the CNS after exposure to anaesthetics .…”

Section: Discussionmentioning

confidence: 99%

“…40 The important contribution of Bcl-2 to apoptotic processes in hippocampal neurons is now especially well documented. 41 Moreover, several studies have linked the reduction of Bcl-2 expression to the neuronal damage in the CNS after exposure to anaesthetics. [42][43][44] Apoptosis is strictly controlled by multiple gene families, including not only the Bcl-2 but also the caspase families.…”

Section: Discussionmentioning

confidence: 99%

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Propofol inhibits proliferation and induces neuroapoptosis of hippocampal neurons in vitro via downregulation of NF‐κB p65 and Bcl‐2 and upregulation of caspase‐3

Zhong

Liang

Chen

et al. 2014

Cell Biochemistry & Function

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Propofol is widely used in paediatric anaesthesia and intensive care unit because of its essentially short-acting anaesthetic effect. Recent data have shown that propofol induced neurotoxicity in developing brain. However, the mechanisms are not extremely clear. To gain a better insight into the toxic effects of propofol on hippocampal neurons, we treated cells at the days in vitro 7 (DIV 7), which were prepared from Sprague-Dawley embryos at the 18th day of gestation, with propofol (0.1-1000 μM) for 3 h. A significant decrease in neuronal proliferation and a remarkable increase in neuroapoptosis were observed in DIV 7 hippocampal neurons as measured by 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyltetrazolium bromide assay and apoptosis assay respectively. Moreover, propofol treatment decreased the nuclear factor kappaB (NF-κB) p65 expression, which was accompanied by a reduction in B-cell lymphoma 2 (Bcl-2) mRNA and protein levels, increased caspase-3 mRNA and activation of caspase-3 protein. These results indicated that downregulation of NF-κB p65 and Bcl-2 were involved in the potential mechanisms of propofol-induced neurotoxicity. This likely led to the caspase-3 activation, triggered apoptosis and inhibited the neuronal growth and proliferation that we have observed in our in vitro systems.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Propofol inhibits proliferation and induces neuroapoptosis of hippocampal neurons in vitro via downregulation of NF‐κB p65 and Bcl‐2 and upregulation of caspase‐3

Zhong

Liang

Chen

et al. 2014

Cell Biochemistry & Function

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“…Ethanol-induced neurotoxicity models have previously been used to study NDDs (Naseer et al, 2014; Saito et al, 2016). In vivo and in vitro studies have shown that chronic ethanol exposure elevates GluN1 and GluN2B gene expression and their polypeptide levels.…”

Section: Glutamate Receptors As Potential Targets In Neurotoxic Agentmentioning

confidence: 99%

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

Jakaria

Park

Haque

et al. 2018

Front. Mol. Neurosci.

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Glutamate receptors play a crucial role in the central nervous system and are implicated in different brain disorders. They play a significant role in the pathogenesis of neurodegenerative diseases (NDDs) such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Although many studies on NDDs have been conducted, their exact pathophysiological characteristics are still not fully understood. In in vivo and in vitro models of neurotoxic-induced NDDs, neurotoxic agents are used to induce several neuronal injuries for the purpose of correlating them with the pathological characteristics of NDDs. Moreover, therapeutic drugs might be discovered based on the studies employing these models. In NDD models, different neurotoxic agents, namely, kainic acid, domoic acid, glutamate, β-N-Methylamino-L-alanine, amyloid beta, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, 1-methyl-4-phenylpyridinium, rotenone, 3-Nitropropionic acid and methamphetamine can potently impair both ionotropic and metabotropic glutamate receptors, leading to the progression of toxicity. Many other neurotoxic agents mainly affect the functions of ionotropic glutamate receptors. We discuss particular neurotoxic agents that can act upon glutamate receptors so as to effectively mimic NDDs. The correlation of neurotoxic agent-induced disease characteristics with glutamate receptors would aid the discovery and development of therapeutic drugs for NDDs.

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“…A recent study in animals showed that plant osmotin can activate a pathway involved in disease resistance by binding to the adiponectin receptors. Through the upregulation of the antiapoptotic Bcl-2 protein, plant osmotin reduces ethanol neurotoxicity and reverses synaptic dysfunction and neuronal apoptosis (Naseer et al 2014 andShah et al 2014). …”

Section: Discussionmentioning

confidence: 99%

“…Osmotin reduces ethanol neurotoxicity via the upregulation of the antiapoptotic Bcl-2 protein, and reverses synaptic dysfunction and neuronal apoptosis. The Bcl-2 protein appears to block a distal step in a common pathway for apoptosis and programmed cell death (Naseer et al 2014 andShah et al 2014). …”

Section: Introductionmentioning

confidence: 99%

Eleven <i>StOSMs</i> Genes in the Potato Genome Response to Water Deficiency

Qiao¹,

Zhang²,

Dai³

et al. 2015

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Osmotin plays an important role in plant response to low temperature and pathogen infection. To date little is known on existence and full function of OSM genes in genome-wide. In this study, based on an OSM expression sequence tag identified from a drought-treated subtractive library, StOSMs in the potato genome were identified and characterized in response to a water deficit gradient. BLAST and bioinformatic analysis revealed that there are at least eleven StOSMs in the potato genome. Among eleven StOSMs, eight StOSM mRNAs accumulated in leaf at the drought-lethal critical point (DLP) were at least 4-fold higher than in the control. The peak StOSM-8E mRNA accumulation was 49-fold higher than the control. Three StOSM mRNAs in leaf at DLP were 9.2-fold lower than in the control. This result of qRT-PCR quantification was identical with the FPKM values of all eleven StOSMs examined in the the Potato Genome Sequence database (PGSD). In conclusion, water deficiency does induce the regulation of the expression of the eleven StOSMs. Either up or downregulated by water deficiency, StOSMs play a positive role in enhancing potato tolerance to drought stress. Therefore, osmotins can be considered to be drought responsive molecules involved in withstanding water deficits. The result provides an evidence to reveal how potato adapts to drought stress.

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Neuroprotective effect of osmotin against ethanol-induced apoptotic neurodegeneration in the developing rat brain

Cited by 56 publications

References 55 publications

Propofol inhibits proliferation and induces neuroapoptosis of hippocampal neurons in vitro via downregulation of NF‐κB p65 and Bcl‐2 and upregulation of caspase‐3

Propofol inhibits proliferation and induces neuroapoptosis of hippocampal neurons in vitro via downregulation of NF‐κB p65 and Bcl‐2 and upregulation of caspase‐3

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

Eleven <i>StOSMs</i> Genes in the Potato Genome Response to Water Deficiency

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